Mutation in the silencing gene SIR4 can delay aging in S. cerevisiae.

Authors: Kennedy BK; Austriaco NR Jr; Zhang J; Guarente L
Year: 1995
Journal: Cell
Abstract: Aging in S. cerevisiae is exemplified by the fixed number of cell divisions that mother cells undergo (termed their life span). We have exploited a correlation between life span and stress resistance to identify mutations in four genes that extend life span. One of these, SIR4, encodes a component of the silencing apparatus at HM loci and telomeres. The sir4-42 mutation extends life span by more than 30% and is semidominant. Our findings suggest that sir4-42 extends life span by preventing recruitment of the SIR proteins to HM loci and telomeres, thereby increasing their concentration at other chromosomal regions. Maintaining silencing at these other regions may be critical in preventing aging. Consistent with this view, expression of only the carboxyl terminus of SIR4 interferes with silencing at HM loci and telomeres, which also extends life span. Possible links among silencing, telomere maintenance, and aging in other organisms are discussed.
Reference

Integration:

Created on Nov. 5, 2012, 4:46 p.m.
Not linked
Integrated: False

No notes
Species: Budding yeast

Experiments: 0
Interventions:

UTH3 deletion

UTH1 deletion

STE12 deletion

sir4-42 mutation

MPT5 deletion

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